Браузер не даёт сохранять данные (например, приватный режим): закладки пропадут после закрытия вкладки.
Поиск статей PubMed
Ключевые слова, автор, журнал, годы — результаты из PubMed, аннотации с переводом на русский, закладки в браузере.
Найдено: 3 200
Страница 90 из 320-
Association between gut microbiota and postpartum depression: A bidirectional Mendelian randomization study.
BACKGROUNDS: Empirical investigations have shown an association between gut microbiota and postpartum depression (PPD); nevertheless, the precise cause-and-effect relationship between these two variables remains ambiguous. This research aimed to examine the possible reciprocal causal relationship between the gut microbiota and PPD. METHODS: In this work, we used Mendelian randomization (MR) to analyze the relationship between the gut microbiota (n = 18,340) and PPD (n = 67,205). We obtained the relevant SNPs from publicly accessible genome-wide association studies (GWAS). The SNP estimations were combined by the inverse-variance weighted (IVW) method, including sensitivity analyses such as weighted median, MR Egger, and MR Pleiotropy Residual Sum and Outlier (PRESSO). RESULTS: We have identified strong correlations between six bacterial characteristics and the likelihood of developing PPD. Our research revealed that the genus Ruminococcaceae UCG010, the family Veillonellaceae, and the class Clostridia had a beneficial effect on preventing PPD. The class Alphaproteobacteria, genus Slackia, and order NB1n were found to have a significant negative impact on PPD. The sensitivity studies conducted on these bacterial features consistently confirmed these finding. LIMITATIONS: It is crucial to acknowledge that our study was conducted just within a European society, which may restrict its applicability to other groups. CONCLUSIONS: The findings from our MR investigation indicate a potential causal relationship between certain kinds of gut bacteria and PPD. Additional investigation is required to elucidate the influence of gut microbiota on the advancement of PPD.
-
Gut microbiota regulates mouse behaviors through glucocorticoid receptor pathway genes in the hippocampus.
Gut microbiota has an important role in the immune system, metabolism, and digestion, and has a significant effect on the nervous system. Recent studies have revealed that abnormal gut microbiota induces abnormal behaviors, which may be associated with the hypothalamic-pituitary-adrenal (HPA) axis. Therefore, we investigated the behavioral changes in germ-free (GF) mice by behavioral tests, quantified the basal serum cortisol levels, and examined glucocorticoid receptor pathway genes in hippocampus using microarray analysis followed by real-time PCR validation, to explore the molecular mechanisms by which the gut microbiota influences the host's behaviors and brain function. Moreover, we quantified the basal serum cortisol levels and validated the differential genes in an Escherichia coli-derived lipopolysaccharide (LPS) treatment mouse model and fecal "depression microbiota" transplantation mouse model by real-time PCR. We found that GF mice showed antianxiety- and antidepressant-like behaviors, whereas E. coli LPS-treated mice showed antidepressant-like behavior, but did not show antianxiety-like behavior. However, "depression microbiota" recipient mice exhibited anxiety- and depressive-like behaviors. In addition, six glucocorticoid receptor pathway genes (Slc22a5, Aqp1, Stat5a, Ampd3, Plekhf1, and Cyb561) were upregulated in GF mice, and of these only two (Stat5a and Ampd3) were upregulated in LPS-treated mice, whereas the shared gene, Stat5a, was downregulated in "depression microbiota" recipient mice. Furthermore, basal serum cortisol levels were decreased in E. coli LPS-treated mice but not in GF mice and "depression microbiota" recipient mice. These results indicated that the gut microbiota may lead to behavioral abnormalities in mice through the downstream pathway of the glucocorticoid receptor. Herein, we proposed a new insight into the molecular mechanisms by which gut microbiota influence depressive-like behavior.
-
Feeling down? A systematic review of the gut microbiota in anxiety/depression and irritable bowel syndrome.
Background Anxiety/depression and irritable bowel syndrome (IBS) are highly prevalent and burdensome conditions, whose co-occurrence is estimated between 44 and 84%. Shared gut microbiota alterations have been identified in these separate disorders relative to controls; however, studies have not adequately considered their comorbidity. This review set out to identify case-control studies comparing the gut microbiota in anxiety/depression, IBS, and both conditions comorbidly relative to each other and to controls, as well as gut microbiota investigations including measures of both IBS and anxiety/depression. Methods Four databases were systematically searched using comprehensive search terms (OVID Medline, Embase, PsycINFO, and PubMed), following PRISMA guidelines. Results Systematic review identified 17 studies (10 human, 7 animal). Most studies investigated the gut microbiota and anxiety/depression symptoms in IBS cohorts. Participants with IBS and high anxiety/depression symptoms had lower alpha diversity compared to controls and IBS-only cohorts. Machine learning and beta diversity distinguished between IBS participants with and without anxiety/depression by their gut microbiota. Comorbid IBS and anxiety/depression also had higher abundance of Proteobacteria, Prevotella/Prevotellaceae, Bacteroides and lower Lachnospiraceae relative to controls. Limitations A large number of gut microbiota estimation methods and statistical techniques were utilized; therefore, meta-analysis was not possible. Conclusions Well-designed case-control and longitudinal studies are required to disentangle whether the gut microbiota is predicted as a continuum of gastrointestinal and anxiety/depression symptom severity, or whether reported dysbiosis is unique to IBS and anxiety/depression comorbidity. These findings may inform the development of targeted treatment through the gut microbiota for individuals with both anxiety/depression and IBS.
-
A food-borne probiotic ameliorates depression by modulating tryptophan metabolism along the gut-brain axis.
Depression is increasingly conceptualized within a neuroimmune framework, where systemic inflammation originating from a compromised gut barrier can drive neuroinflammation and behavioral deficits. This study investigated whether the probiotic Weizmannia coagulans BC99 exerts antidepressant effects by modulating this gut-immune-brain axis. In a chronic unpredictable mild stress (CUMS) rat model, BC99 supplementation significantly alleviated depressive-like behaviors. Our integrated multi-omics analysis suggests a sequential mechanistic cascade. BC99 first partially restored intestinal barrier integrity, upregulating tight junction proteins (ZO-1, Occludin). This was associated with a marked attenuation of peripheral and hippocampal pro-inflammatory cytokines (IL-23, IFN-γ) and oxidative stress. Concurrently, hippocampal metabolomics showed BC99 shifted tryptophan metabolism from the immune-activated, neurotoxic kynurenine pathway toward the neuroprotective serotonin pathway. Integrated hippocampal transcriptomics and proteomics identified the activation of the BDNF/TrkB/CREB neurotrophic signaling pathway and upregulation of synaptic plasticity proteins (SYN, PSD-95) as central downstream events. These findings outline a potential gut-immune-brain mechanism: BC99-initiated gut barrier repair dampens systemic inflammation, which in turn resolves neuroinflammatory tone and rebalances neurochemistry, ultimately fostering a hippocampal milieu conducive to neuroplasticity and behavioral resilience.
-
Gut Microbiota-driven Tryptophan Metabolism Towards the Indole Pathway Mediates Schisandra Chinensis Polysaccharide's Alleviation of Ulcerative Colitis and Comorbid Depression via Aryl Hydrocarbon Receptor.
Patients with ulcerative colitis (UC) exhibit heightened depression risk, linked to microbiota-gut-brain axis dysfunction. This study isolated a novel low-molecular-weight Schisandra chinensis polysaccharide (SCP) that ameliorated UC and comorbid depression by remodeling gut microbiota, redirecting tryptophan (Trp) metabolism toward the indole pathway, and activating aryl hydrocarbon receptor (AhR). Structurally, SCP features a →4)-α-D-Glcp backbone with O-6 branched chains. In dextran sulfate sodium-induced UC mice, SCP mitigated colonic inflammation, restored intestinal barrier integrity, and improved depression-like behaviors by repairing blood-brain barrier, reducing neuroinflammation, preserving hippocampal neurons, and modulating synaptic plasticity. Multi-omics revealed SCP enriched beneficial microbiota (e.g., Limosilactobacillus reuteri) and rebalanced Trp metabolism along the gut-brain axis. SCP suppressed the hyperactive kynurenine (Kyn) pathway (reduced Kyn/Trp ratio) while elevating indole-3-propionic acid (IPA) levels in colon, serum, and hippocampus. Functioning as a pivotal molecule, IPA exerted dual anti-inflammatory effects in both colon and hippocampus via AhR activation and NF-κB inhibition. Antibiotic depletion and fecal microbiota transplantation validated SCP's microbiota-dependent efficacy, while IPA supplementation recapitulated SCP's benefits. AhR inhibition abolished SCP's therapeutic actions, confirming AhR as the critical target. Collectively, these findings propose a novel therapeutic strategy for UC and associated depression, highlighting SCP's potential value in targeting the Trp metabolism-AhR axis.
-
Omega-3 polyunsaturated fatty acids critically regulate behaviour and gut microbiota development in adolescence and adulthood.
BACKGROUND: Neurodevelopment is strongly influenced by maternal and early-postnatal diet. Omega-3 polyunsaturated fatty acids (n-3 PUFA) are vital structural and functional components of the developing brain. The gut microbiota is also influenced by n-3 PUFA status, however, little is known about the role of maternal and early-life n-3 PUFA intake on offspring gut microbiota development and subsequent interactions with central nervous system functioning and behavioural outcomes. METHODS: Pregnant female C57BL/6 mice and their male offspring were fed a control (CON), omega-3 deficient (O3-) or omega-3 supplemented (O3+) diet. Cognitive, depressive and social behaviours were assessed through a battery of behaviour tests in the male offspring at both adolescence (week 4-5) and adulthood (week 11-13). Hypothalamic-pituitary-adrenal axis (HPA) activation was assessed by analysis of stress-induced corticosterone production. Fecal microbiota composition was analysed by 16S sequencing at both adolescent and adulthood. In addition, stimulated spleen cytokine levels were assessed. RESULTS: n-3 PUFA interventions induced subtle changes in offspring early-life and adolescent behaviours, which were further evident in adulthood, such that O3- animals displayed impaired communication, social and depression-related behaviours and O3+ animals displayed enhanced cognition. O3- mice displayed an elevated Firmicutes:Bacteroidetes ratio and blunted systemic LPS responsiveness. Contrastingly, O3+ mice displayed greater fecal Bifidobacterium and Lactobacillus abundance and dampened HPA-axis activity. CONCLUSIONS: Neurobehavioural development related to cognitive, anxiety and social behaviours, is highly dependent upon in utero and lifelong n-3 PUFA availability. In addition, neurobehavioural changes induced by altering n-3 PUFA status are closely associated with comprehensive alterations in gut microbiota composition, HPA-axis activity and inflammation.
-
Peach Gum Polysaccharide Prevents Chemotherapy-Induced Intestinal Injury and Degenerative Behavior.
This study investigated the effects of peach gum polysaccharide (PGP) on chemotherapy-induced intestinal injury and behavioral changes in mice. Female C57BL/6 mice were injected with E0771 breast cancer cells and divided into 3 groups: control, chemotherapy (pirarubicin), and PGP treatment (pirarubicin plus PGP). Behavioral tests, colon length measurement, tissue staining, 16S rDNA sequencing, and metabolomics were performed. Transcriptomic data of colon and hippocampal tissues were analyzed and validated by Western blotting. PGP significantly alleviated colon damage, reduced inflammation and apoptosis, and restored colon length. It mitigated depressive behaviors by suppressing inflammasome activation in the hippocampus, increased gut microbiota diversity, and improved depression-associated metabolites. After the depletion of the intestinal flora, the antidepressant effect of PGP is significantly weakened. These findings suggest that PGP protects against chemotherapy-induced intestinal and behavioral damage by modulating the gut microbiota and gut-brain axis.
-
Polysaccharide PSLP-1 from Polygonatum sibiricum Stems and Leaves Alleviates Depressive-like Behaviors and Modulates Gut Microbiota and Tryptophan Metabolism along the Gut-Brain Axis.
The stems and leaves of Polygonatum sibiricum Red. are underused food byproducts whose polysaccharides and bioactivities remain poorly characterized. In this study, a novel homogeneous polysaccharide, PSLP-1 (4.287 kDa), was isolated and identified as a fructan-rich fraction with a →1)-β-d-Fruf-(2→ backbone and C6 side-chain substitution. In a chronic restraint stress mouse model, PSLP-1 showed clear antidepressant-like activity by reducing immobility time in both the forced swim and tail suspension tests. PSLP-1 was also associated with restoration of tryptophan metabolism, characterized by suppression of the indoleamine 2,3-dioxygenase 1-mediated kynurenine pathway and promotion of tryptophan hydroxylase-related 5-hydroxytryptamine synthesis. These effects were accompanied by gut microbiota remodeling, including increased Akkermansia and decreased Lactobacillus and Alistipes. These findings support P. sibiricum stems and leaves as a promising source of bioactive polysaccharides.
-
Caffeine plays a prevention role in stress-induced depression by modulating gut-brain axis function.
BACKGROUND: Caffeine intake is inversely associated with depression in epidemiological studies and can impact gut microbiota. Considering the close relationship between depression and gut microbiota, we conducted this study to investigate whether prophylactic caffeine use could influence the development of depression by affecting gut-brain axis. METHODS: Male C57BL/6J mice were randomly divided into three groups: a control group, one group receiving chronic unpredictable stress (CUS) as CUS group, and one group receiving CUS after intraperitoneal injection with caffeine (CAF) as CAF group. Depressive- and anxiety-like behaviors were assessed, and gut-brain axis related molecules were examined. RESULTS: Compared to control group, CUS group had significantly lower body weight, sucrose preference, center distance (%) and higher immobility time; however, the values of these indexes were similar between control group and CAF group. Furthermore, the significantly decreased intestinal barrier integrity-related factors (Zonula Occludens-1 (ZO-1), claudin-1 and Mucin2 (MUC2)) in CUS were not observed in CAF group; and the altered levels of two inflammation factors in plasma (lipopolysaccharide (LPS) and NOD-like receptor thermal protein domain-associated protein 3 (NLRP3)) and four inflammation-related factors in hippocampus (tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), adenylyl cyclase (AC) and brain-derived neurotrophic factor (BDNF)) in CUS group were not observed in CAF group. In addition, we found that six differential genera were identified between control group and CUS group, but not between control group and CAF group; and sucrose preference were significantly correlated with five of these six differential genera. CONCLUSIONS: The results suggested that early caffeine intervention might prevent depression by regulating gut microbiota, intestinal barrier integrity and neuroinflammation.
-
Modulating Gut Microbiota with Dietary Components: A Novel Strategy for Cancer-Depression Comorbidity Management.
BACKGROUND: Gut microbiota play a critical role in mediating the bidirectional association between cancer and depression. Emerging evidence indicates that adjusting the dietary component intake can significantly alter gut microbiota composition, thereby influencing the host's metabolism and immune function. Changes in gut microbiota and their metabolites may represent key factors in preventing cancer-depression comorbidity. METHODS: English publications were searched in databases including the Web of Science, Scopus, and PubMed using a series of keywords: "cancer", "depression", "gut microbiota", "dietary components", and related terms, individually or in combination. The search focused on preclinical and clinical studies describing the regulatory effects of dietary component interventions. RESULTS: This narrative review summarizes the associations among gut microbiota, cancer, and depression, and synthesizes current evidence on the modulatory effects and mechanisms of specific dietary component interventions, including dietary patterns, probiotics, prebiotics, and diet-derived phytochemicals, on gut microbiota. On the one hand, these interventions inhibit abnormal proliferation signals in the tumor microenvironment and enhance anticancer immune responses; on the other hand, they modulate neurotransmitter homeostasis, suppress neuroinflammation, and improve mood behaviors through the gut-brain axis interactions mediated by microbial metabolites. CONCLUSIONS: The complex associations among cancer, depression, and gut microbiota require further clarification. Modulating gut microbiota composition through dietary components represents a novel therapeutic strategy for improving cancer-depression comorbidity. Regulated gut microbiota enhance immune homeostasis and intestinal barrier function, while their metabolites bidirectionally modulate one another via systemic circulation and the gut-brain axis, thereby improving both the tumor microenvironment and depressive-like behaviors in cancer patients while reducing the adverse effects of cancer.